Defective DNA repair has been related to carcinogenesis by the demonstration that cells of patients with xeroderma pigmentosum are unable to repair the damage of UV radiation. Xeroderma Pigmentosum is characterized by extreme photosensitivity and the development of malignant skin tumors. Our laboratory has been investigating the effect of a chemical on DNA repair. The substance is phorbol myristate acetate, a potent cocarcinogen (promoting agent). Cocarcinogens stimulate the development of tumors in animals previously exposed to subtumorigenic doses of a known carcinogen. The question asked is whether the cocarcinogen inhibits DNA repair. Were this so, one could postulate that inhibition of repair of damage to DNA by the carcinogen was effected by the cocarcinogen thereby leading to the appearance of tumors. We have shown that the cocarcinogen does inhibit the repair of UV damage to HeLa cells by preventing excision of the photoproduct, pyrimidine dimers, from the DNA. The mechanism of this inhibition is under investigation.